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Flashcards in Cardiovascular disease Deck (27)
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1
Q

2 things that cause inadequate supply to the myocardium

A

Reduced coronary blood flow

Myocardial hypertrophy

2
Q

4 IHD syndromes

A

Anigna pectoris
Acute coronary syndrome
Sudden cardiac death
Chronic ischaemic heart disease

3
Q

3 types angina

A

Stable- predictable relationship with exertion, due to fixed obstruction
Unstable- plaque disruption, red flag
Varient/prinzmetal- coronary artery spasm

4
Q

2 ways a subendocardial MI might occur without any acute coronary occlusion?

A
  1. Stable athromatous occlusion

2. acute hypotensive episode

5
Q

Main blood marker of cardiac myocyte damage?

A

Troponins T and I

6
Q

When is troponin peaked?

A

12hrs post MI

7
Q

What else is troponin raised in?

A

PE, HF, myocarditis

8
Q

4 other blood markers of cardiac myocyte damage?

A

Creatinine kinase MB
Myoglobin
Lactate dehydrogenase
Aspartate transaminase

9
Q

What is Dressler’s syndrome?

A

Complication of MI- autoimmune pericarditis.

10
Q
Appearance of heart tissue following MI:
Less than 24 hours
1-2 days
3-4 days
1-3 weeks
More than 3 weeks
A

Less than 24 hours normal/dark
1-2 days pale, oedema
3-4 days yellow with haemorrhagic edges (macrophages)
1-3 weeks red/grey, pale, thin, granulation tissue then fibrosis
More than 3 weeks dense fibrous scar

11
Q

What is chronic ischaemic heart disease?

A

Atheroma = relative ischaemia and angina. Risk of sudden death, MI, unstable/variant angina

12
Q

2 most common mutations in familial hypercholesterolaemia

A

Low density lipoprotein receptor gene

Apolipoprotein B

13
Q

How do heterozygotes with familial hypercholesterolaemia present?

A

Xanthomas

Early atherosclerosis

14
Q

What BP is definted as HTN

A

140/90

15
Q

What do all primary/essential HTN causes have in common?

A

Positive sodium balance

16
Q

How does sodium increase BP?

A

Increases stroke vol as more water in blood, cardiac output is therefore increased, so vasoconstriction occurs to reduce the blood flow as is above metabolic demand, however this increases SVR so BP (SVRxCO) increases.

17
Q

4 systems that if diseased might cause secondary HTN?

A

Renal
Endocrine
Cardio
Neuro

18
Q

4 effects of hypertension

A

Renal failure
Hypertensive crisis
Acute hypertensive encephalopathy
Pulmonary HTN

19
Q

What BP is a HTNve crisis?

A

180/120

20
Q

Symptoms of acute hypertensive encephalopathy

A

Confusion, vomiting, convulsions, coma, death

21
Q

Framingham study was on what?

A

Risk factors for heart disease

22
Q

Describe RAAS?

A

angiotensin produced in afferent arterioles of kidney
Renin converts angiotensin to angiotensin I
Angiotensin I to angiotensin II
Ang 2 = vasoconstriction and stimulates adrenals to produce aldosterone
Aldosterone inhibits sodium and water loss to increase blood volume.

23
Q

What is Conn’s syndrome

A

Excess aldosterone secretion usually due to adrenocortical adenoma
HTN
elevated aldosterone, low renin
Potassium loss- muscle weaknessm arrhythmias, parasthaesia, metabolic alkalosis

24
Q

What is phaeochromocytoma

A

Tumour of adrenal medulla, secretes vasoconstrictive catecholamines (adrenaline and noradrenaline)
Presents with pallor, headache, sweating, nervousness, HTN

25
Q

Difference between Cushing’s disease and syndrome

A
Disease= pituitary lesion or neoplasm in adrenals that results in overproduction of glucocorticoids
Syndrome = excess glucocorticoids from any source
26
Q

What is the action of cortisol?

A

Sympathetic NS activation

Acts on the kidneys to = HTN

27
Q

3 causes of Cushing’s

A

Adrenocortical adenoma (or other neoplasm)
Pituitary adenoma
Paraneoplastic effect of other neoplasms (particularly small cell lung carcinoma) producing adrenocorticotrophic hormone that stimulates adrenals to produce cortisol